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Participation of the components of L-arginineitric oxide/cGMP cascade by chemically-induced abdominal constriction in the mouse.

机译:化学诱导的小鼠腹部收缩使L-精氨酸/一氧化氮/ cGMP级联的成分参与。

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摘要

The purpose of this study was to investigate the role of the L-arginineitric oxide (NO)/cGMP pathway in p-benzoquinone-induced writhing model in mouse. L-arginine, a NO precursor, displayed antinociceptive effects at the doses of 0.125-1.0 mg/kg. When the doses of L-arginine were increased gradually to 10-100 mg/kg, a dose-dependent triphasic pattern of nociception-antinociception-nociception was obtained. The NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (18.7515 mg/kg), possessed antinociceptive activity. Methylene blue (MB), a guanylyl cyclase and/or NOS inhibitor, (5-160 mg/kg) also produced a dose-dependent triphasic response. When L-arginine (50 mg/ kg) was combined with L-NAME (75 mg/kg). L-arginine-induced antinociception did not change significantly. Cotreatment of L-arginine with 5 mg/kg MB significantly decreased MB-induced antinociception and reversed the nociception induced by 40 mg/kg MB to antinociception. It is concluded that the components of L-arginineitric oxide/cGMP cascade may participate in nociceptive processes both peripherally and centrally by a direct effect on nociceptors or by the involvement of other related pathways of nociceptive processes induced by NO.
机译:这项研究的目的是调查L-精氨酸/一氧化氮(NO)/ cGMP途径在对苯醌引起的小鼠扭体模型中的作用。 NO的前体L-精氨酸在0.125-1.0 mg / kg的剂量下显示出抗伤害作用。当L-精氨酸的剂量逐渐增加至10-100mg / kg时,获得了伤害-痛觉-伤害感受的剂量依赖性三态模式。 NO合酶(NOS)抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)(18.7515 mg / kg)具有抗伤害感受活性。亚甲基蓝(MB),鸟苷酸环化酶和/或NOS抑制剂(5-160 mg / kg)也产生剂量依赖性的三相反应。将L-精氨酸(50 mg / kg)与L-NAME(75 mg / kg)合并使用时。 L-精氨酸诱导的抗伤害感受没有明显改变。 L-精氨酸与5 mg / kg MB的共处理可显着降低MB诱导的抗伤害感受,并将40 mg / kg MB诱导的伤害感受转化为抗伤害感受。结论是,L-精氨酸/一氧化氮/ cGMP级联的成分可能通过直接影响伤害感受器或通过NO诱导的伤害感受过程的其他相关途径参与而在外周和中央参与伤害感受过程。

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